Qhov tshwm sim ntawm mob raum mob hnyav: Yuav Ua Li Cas Sib Txawv?
Mar 16, 2022
Hu rau: Audrey Hu Whatsapp / hp: 0086 13880143964 Email:audrey.hu@wecistanche.com
Matthieu Jamme et al
Abstract
Keeb kwm: mob raumraug mob(AKI) yog ib qho ntawm feem ntau lub cev tsis ua haujlwm tau ntsib ntawm cov neeg mob hnyav. Ntxiv rau cov teeb meem tam sim no uas paub zoo (hydro electrolytic disorders, hypervolemia, kev siv tshuaj ntau dhau), qhov tshwm sim ntawm cov teeb meem mus sij hawm ntev thiab / lossis mob ntev uas cuam tshuam nrog AKI tau raug kwv yees ntev. Lub hom phiaj ntawm cov ntawv sau no yog los tshuaj xyuas luv luv thiab lub sijhawm ntev ntawm AKI thiab sib tham txog cov tswv yim uas yuav txhim kho cov txiaj ntsig ntawm AKI.
Lub cev tseem ceeb:Peb tau tshuaj xyuas cov ntaub ntawv, tsom mus rau qhov tshwm sim ntawm AKI hauv txhua yam thiab kev tswj hwm ntawm AKI. Peb tau hais txog qhov tseem ceeb ntawm kev tswj xyuas kev kho mob rau kev txhim kho cov txiaj ntsig AKI. Thaum kawg, peb kuj tau npaj cov neeg sib tw 'cov tswv yim yav tom ntej thiab kev tswj hwm kev xav.
Xaus:AKI yuav tsum raug suav hais tias yog kab mob. Vim nws qhov cuam tshuam luv luv thiab ntev, kev ntsuas los tiv thaiv AKI thiab txwv qhov tshwm sim ntawm AKI yuav tsum txhim kho thoob ntiaj teb cov txiaj ntsig ntawm cov neeg mob uas muaj mob hnyav.
Ntsiab lus: Mob hnyavraum raug mob, Cov txiaj ntsig ntev,Ntevraumkab mob, Kev kho mob hnyav

Cistanche deserticola tiv thaiv kab mob raum, nyem qhov no kom tau txais cov qauv
Taw qhia
Mob raum raug mob (AKI) yog ib qho ntawm feem ntau lub cev tsis ua haujlwm tau ntsib hauv cov tsev kho mob hnyav (ICU). Txij li thaum nws thawj lub ntsiab lus los ntawm Homer W. Smith nyob rau hauv lub fifties [1], ntau tshaj 30 ntau lub ntsiab txhais tau siv, ua rau ib tug loj epidemiological heterogeneity [2] nrog tshwm sim li ntawm 5 [3] mus rau 25 feem pua [4].
Txij li xyoo 2004, peb lub ntsiab lus, raws li cov ntshav creatinine (SCr) thiab cov zis tso zis, raws li: RIFLE [5], AKIN [6], thiab qhov tseeb KDIGO kev faib tawm [7] tau raug tso cai tso cai rau homogenization ntawm AKI txhais raws li kev sib kis. Kev koom tes ntawm AKI thiab mob raum mob (CKD). Raws li cov lus txhais KDIGO tam sim no, AKI tshwm sim ntau tshaj li ib feem peb ntawm cov neeg mob ICU [8, 9].
Vim li cas cov kws kho mob yuav tsum txhawj xeeb txog AKI?
Qhov tshwm sim ntawm AKI sawv cev rau qhov kev ntsuas ntse ntse rau cov neeg mob los ntawm kev cuam tshuam rau ob qho tib si luv luv thiab ntev mus ntev.
AKI thiab thoob ntiaj teb (luv luv thiab ntev) prognosis
Txoj kev tshawb fawb multinational EPI-AKI tau taw qhia tias AKI tau cuam tshuam nrog kev tuag luv luv hauv kev mob hnyav (LOSSIS=2.19 [1.44–3.35], 3.88 [2.42–6.21] thiab 7.18 [5.13–10.04 ] rau KDIGO theem 1, 2 thiab 3, ntsig txog) [8]. Txhua pab pawg ntawm ICU cov neeg mob zoo li cuam tshuam [10–15]. Qhov tsis zoo luv luv- thiab qhov txiaj ntsig nruab nrab ntawm lub sijhawm kuj tau pom nyob rau hauv cov neeg mob uas muaj subclinical AKI (txhais los ntawm biomarkers zoo ntawm lub raum raug mob tab sis tsis ua raws li cov ntsiab lus tam sim no ntawm AKI) [16].
Ntxiv mus, AKI tau rov ua dua nrog cov txiaj ntsig tsis zoo rau lub sijhawm ntev [17]. Hauv kev tshawb fawb loj tshaj tawm txog 1-xyoo qhov txiaj ntsig ntawm ntau dua 16,000 cov neeg mob tau tawm hauv tsev kho mob thiab leej twg raug mob AKI hauv ICU, tsib qhov profile tau txheeb xyuas raws li lub raum mob thaum lub sij hawm ICU thiab nyob hauv tsev kho mob. : cov neeg mob ntxov (<7 days="" from="" admission)="" or="" late="" (="">7 hnub) kev rov qab zoo, rov qab los nrog (rov qab tsis zoo) lossis tsis hloov lub raum ua haujlwm hauv tsev kho mob tawm (rov qab rov qab) thiab lub raum tsis ua haujlwm [18]. Cov neeg mob uas hloov lub raum ua haujlwm ntawm lub tsev kho mob tawm (tsis rov qab los yog rov qab tsis tau rov qab los) tau txais qhov tshwm sim tsis zoo. Interestingly, txawm tias cov neeg mob uas pom tau zoo los ntawm AKI ntawm ICU tso tawm (raws li cov ntshav creatinine) tab sis nrog cov biomarkers zoo ntawm lub raum raug mob muaj kev pheej hmoo ntawm kev tuag ntau dua thaum lub xyoo tom qab ICU tso tawm. Ib zaug ntxiv, qhov no qhia tias dhau ntawm qhov cuam tshuam ntawm lub raum tsis ua haujlwm, lub raum puas cuam tshuam rau lub sijhawm ntev [19].

Cistanche muaj txiaj ntsig zoo rau mob raum
AKI thiab mob raum mob (CKD) Te kawg ntawm 2010s tau raug cim los ntawm kev tshaj tawm ntawm ntau qhov kev tshawb fawb uas tau qhia txog kev koom tes ntawm AKI thiab tom qab CKD tshwm sim. Wald et al. tau muab piv rau 3,769 rau 13,598 tus neeg mob sib tw kho lossis tsis kho nrog raum hloov kho (RRT) hauv ICU thiab pom qhov tshwm sim ntau dua ntawm cov kab mob raum kawg nrog RRT (2.63 vs. 0.91/100 tus neeg mob-xyoo, kev phom sij ntau dua{12} }.23 [2.70–3.{17}}]) [20]. Hauv ib lub tebchaws Swedish ntawm 97,782 tus neeg mob ICU, Rimes-Stigare li al. tau tshaj tawm tias cov neeg mob uas raug kev txom nyem de novo AKI muaj kev pheej hmoo ntawm CKD (kho qhov xwm txheej tus nqi sib piv=7.6 [95 feem pua CI 5.5–10.4]) thiab cov kab mob hauv lub raum kawg (ESRD) (kho qhov xwm txheej piv txwv =22.5 [95 feem pua CI 12.9–39.1]) piv rau cov neeg mob uas tsis muaj AKI thaum lawv nyob hauv ICU [21]. Tib pab pawg tau txheeb xyuas tias CKD ntawm ICU nkag thiab qhov hnyav ntawm AKI tau cuam tshuam nrog ESRD hauv 1- xyoo muaj sia nyob [22]. Cov kev soj ntsuam zoo sib xws tau ua nyob rau hauv cov pab pawg tshwj xeeb xws li cov neeg laus [23], menyuam yaus [24], mob ntshav qab zib [25], tom qab phais plawv [26], lossis cov neeg mob plawv nres [27].
Interestingly, cov neeg mob uas zoo tag nrho ntawm lub tsev kho mob tso tawm tseem muaj kev pheej hmoo ntawm CKD 1 xyoo tom qab ntawd, tshwj xeeb tshaj yog nyob rau hauv cov ntaub ntawv tom ntej ntawm AKI thaum lub sij hawm ICU nyob [18]. Nco ntsoov, tag nrho cov kev tshawb fawb no tau rov qab los lossis muab cov txiaj ntsig los ntawm kev tswj hwm cov ntaub ntawv hluav taws xob uas muaj kev pheej hmoo loj ntawm kev tsis ncaj ncees. Ib txoj kev tshawb fawb tseem ceeb tsis ntev los no tau qhia meej txog kev koom tes ntawm AKI thiab CKD. Hauv Kev Ntsuam Xyuas, Kev Ntsuam Xyuas Serial, thiab Tom Qab Sequelae IN Acute Kidney Injury (ASSESS-AKI) Txoj Kev Kawm, ib qho kev tshawb fawb ntau dua piv rau 769 cov neeg mob uas muaj lossis tsis muaj AKI, cov kws sau ntawv tau pom tias qhov nce ntxiv ntawm cov zis albumin-to-creatinine (ACR) piv ntawm 3 lub hlis tom qab tso tawm yog qhov kev kwv yees tshaj plaws ntawm biomarker ntawm lub raum kev loj hlob (HR=1.25 [1.10–1.43] ib ob npaug ntawm cov zis ACR, P<0.001). interestingly,="" in="" multivariable="" analysis,="" aki="" occurrence="" was="" not="" associated="" with="" kidney="" disease="" progression="" [28].="" however,="" we="" should="" not="" neglect="" the="" importance="" of="" aki="" in="" the="" evaluation="" of="" renal="" prognosis="" regards="" to="" the="" sensitivity="" analyses="" performed="" using="" the="" urine="" protein-to-creatinine="" ratio="" instead="" of="" urine="" acr.="" in="" that="" case,="" aki="" became="" strongly="" associated="" (hr="2.53" [1.21–5.25],="" p="0.01)" with="" kidney="" disease="" progression.="" moreover,="" the="" c="" statistic="" used="" to="" discriminate="" the="" risk="" of="" poor="" renal="" outcome="" was="" better="" in="" the="" latter="" (0.84="" vs="">0.001).>
Peb qhov kev nkag siab tam sim no yog tias qhov mob hnyav tawm ntawm qhov tsis txaus ntseeg (uas xav tias yuav yog, lom neeg, ntawm epigenetic xwm) tuaj yeem txhawb lub raum fibrosis [29, 30]. Txawm li cas los xij, cov txheej txheem ua rau CKD hauv cov ntsiab lus no tseem tsis tau nkag siab tag nrho.
AKI thiab kev pheej hmoo mob plawv mus sij hawm ntev Hauv ntau qhov kev tshawb fawb loj loj, AKI tau cuam tshuam nrog kev pheej hmoo siab ntawm cov hlab plawv [31–33], tshwj xeeb tshaj yog lub plawv tsis ua haujlwm. Hauv kev tshawb xyuas meta-tshaj tawm tsis ntev los no, Otudayo li al. qhia txog 58 feem pua , 40 feem pua , thiab 15 feem pua nce kev pheej hmoo ntawm lub plawv tsis ua hauj lwm, myocardial infarction, thiab mob stroke, feem [34]. Mechanisms ua rau cov xwm txheej hauv plawv tsis tau piav qhia txog tam sim no. Accelerated atherosclerosis tej zaum yuav yog ib qho txiaj ntsig [35]. Hauv kev tshawb nrhiav kev txhais lus ua nyob rau hauv 968 cov neeg laus tau txais kev phais mob plawv, cov neeg mob nrog kev kho mob AKI, thiab kev mob plawv siab biomarkers nyob rau hnub 1-3 tau cuam tshuam nrog kev mob plawv mus sij hawm ntev. Lwm cov txheej txheem cuam tshuam nrog mitochondrial dysregulation kuj tau pom zoo. Sumida et al. pom muaj zog cardiomyocyte apoptosis thiab mob plawv tsis ua haujlwm tom qab lub raum ischemia-reperfusion hauv tus qauv nas. Cov kws sau ntawv kuj tau pom qhov nce ntxiv ntawm mitochondrial fragmentation hauv cardiomyocytes nrog rau kev sib sau ntawm ib qho tshwj xeeb fission regulation protein: Drp1 [36].
Hauv qhov sib piv, urinary raum raug mob biomarkers ntawm hnub 1-3 tsis cuam tshuam nrog qhov tshwm sim [37]. Cov txiaj ntsig no tau qhia tias AKI yog qhov qhia txog kev ntxhov siab hauv plawv es tsis yog txoj hauv kev rau lub raum. Txawm li cas los xij, kev koom tes ntawm qhov tshwm sim ntawm cov xwm txheej ntawm cov hlab plawv thiab AKI tseem tshuav tom qab hloov kho rau cov kab mob plawv thiab cov ntaub ntawv kho mob tau sib cav txog qhov cuam tshuam ncaj qha ntawm AKI ntawm kev puas tsuaj rau cov hlab plawv [38].
Qhov kev xav no kuj tau tshwm sim hauv kev sim ua haujlwm murine hais txog lub luag haujlwm ntawm galectin -3 txoj hauv kev [39]. Prudhomme et al. muaj pov thawj AKI nce galectin -3 qhia, uas ua rau mob plawv nrog macrophage infiltration thiab plawv fibrosis ua rau lub plawv tsis ua haujlwm.

Cistanche muaj txiaj ntsig zoo hauv kev kho mob raum
Peb theem tseem ceeb ntawm kev tswj lub raum: ua ntej, thaum, thiab tom qab AKI (Fig. 1)
Ua ntej AKI: tiv thaiv AKI tshwm sim
Lub hauv paus ntawm kev tiv thaiv AKI hauv ICU cov neeg mob yog kev tswj hwm ntawm hemodynamics, suav nrog cov ntim tsim nyog, xaiv cov kua dej, thiab cov tshuaj vasoactive. Txawm hais tias qhov pathogenesis ntawm AKI hauv ICU cov neeg mob tuaj yeem tso siab rau cov txheej txheem sib txawv [8, 40], hemodynamic optimization zoo li tseem ceeb los tiv thaiv kev hloov pauv ntawm lub raum ntshav khiav (RBF) [41].
Kev tswj hwm hemodynamic Kev hloov ntim tsim nyog yuav tsum tau ua kom ntxov li sai tau thaum nco ntsoov tias cov kua dej ntau dhau tau tshaj tawm tias muaj feem cuam tshuam nrog cov neeg mob tsis zoo hauv AKI [42, 43]. Qhov kev soj ntsuam antagonist pom tseeb no yuav qhia txog qhov hnyav dua ntawm AKI cov neeg mob xav tau cov kua dej ntau dua thiab lub luag haujlwm tseem ceeb ntawm lub sijhawm ntawm kev tswj hwm cov kua dej thaum lub sijhawm muaj mob hnyav. Txij li thawj qhov kev ceeb toom tshaj tawm txog nephrotoxicity ntawm cov khoom siv dag zog colloids [44, 45], txawm hais tias tej zaum tsis tshua muaj kev phom sij rau cov neeg mob hnyav [46], crystalloids yog cov kev xaiv rau cov neeg mob ICU [47, 48]. Cov txiaj ntsig tsis ncaj thiab cov kev soj ntsuam pom tau pom tias muaj txiaj ntsig zoo rau lub raum nrog lub npe hu ua cov tshuaj sib npaug [49, 50]. Qhov no tuaj yeem tau piav qhia los ntawm kev cuam tshuam loj heev ntawm hyperchloremia acidosis tshwm sim los ntawm kev daws teeb meem ntau hauv chlorine [51]. Yog tias cov kev soj ntsuam no tsis tuaj yeem txheeb xyuas los ntawm qhov kev sim tshuaj ntsuam xyuas randomized SPLIT (tus txheeb ze pheej hmoo rau AKI tshwm sim hauv 90 hnub=1.04 [0.80–1.36] , p=0.77), qhov tsis muaj qhov piv txwv loj suav ntxiv rau kev tswj hwm tsis muaj kev tswj hwm ntawm cov tshuaj ua ntej nkag mus rau ICU txwv kev txhais cov txiaj ntsig no [52]. Hauv Isotonic Solutions thiab Major Adverse Renal Events Trial (SMART) hauv ICU thiab cov neeg mob uas tsis yog-ICU, kev tiv thaiv lub raum muaj txiaj ntsig zoo rau kev siv cov tshuaj sib npaug nrog kev txo qis hauv kev pheej hmoo ntawm lub raum tsis zoo los ntawm 1.1 [1.092–1.107] feem pua ntawm cov neeg mob ICU thiab 0.9 [0.889–0.911] feem pua rau cov neeg mob uas tsis yog ICU [53, 54] tau pom. Txawm li cas los xij, nws yog ib qho tseem ceeb uas yuav tsum nco ntsoov tias qhov ntsuas qhov tsis txaus ntseeg tau suav rau cov kev tshawb fawb SMART, uas yog ib qho ntxiv rau p-tus nqi rau kev txhais cov txiaj ntsig ntawm kev sim tshuaj ntsuam xyuas, tsawg heev. Qhov kev soj ntsuam no qhia txog qhov tsis muaj zog ntawm cov txiaj ntsig [55]. Tab sis qhov frailty index kuj tseem tuaj yeem txhais tau raws li qhov kev xav ntawm qhov kev xaiv zoo ib yam ntawm qhov loj ntawm cov pej xeem tau kawm txog qhov loj ntawm cov nyhuv pom. Thaum kawg, nws siv tsis ntev los no tau sib cav vim tias nws tau raug pov thawj tias tsis muaj peev xwm ntawm qhov frailty index los ntsuas qhov sib txawv ntawm tus qauv qhov kev xav [56]. Txawm hais tias qhov sib npaug ntawm crystalloids vs ib txwm saline tsis raug kaw, accumulating pov thawj qhia tau hais tias (1) ib txwm saline tsis zoo tshaj rau cov tshuaj sib npaug thiab (2) cov kev daws teeb meem yuav zoo dua rau cov saline ib txwm nyob rau hauv cov neeg mob hnyav thiab mob hnyav. . Tseem tos cov kev sim siab tsis tu ncua, qhov no ua pov thawj hauv peb qhov kev pom kev siv cov kev daws teeb meem zoo li cov kua dej thawj zaug hauv ICU cov neeg mob.
Dhau li ntawm qhov kev xaiv ntawm solute, lub tswv yim ntawm qhov zoo tshaj plaws txhais tau tias lub hom phiaj ntawm lub siab arterial siab tau tawm tswv yim rau lub sijhawm ntev. Hauv EPI-AKI txoj kev tshawb fawb, cov xwm txheej cuam tshuam nrog AKI suav nrog keeb kwm kev kho mob yav dhau los ntawm kev kub siab lossis kev poob siab ntawm ICU nkag, nrog rau cov qhab nia siab dua qhov mob physiology 3 [8]. Cov txiaj ntsig no tau ua raws li cov kev sim SEPSIS-PAM [57]. SEPSIS-PAM yog ib qho randomized tswj kev sim (RCT) lub hom phiaj ntawm lub siab ntawm cov hlab ntsha ntawm 65 lossis 85 mmHg. Nws pom tau tias muaj qhov txo qis ntawm AKI hnyav thiab tus nqi ntawm lub raum hloov kho hauv cov neeg mob uas muaj ntshav siab nyob rau hauv cov ntshav siab siab (31 vs. 42 feem pua, p=0.04) [57]. Qhov kev sib raug zoo no tau pom nyob rau hauv cov kev tshawb fawb physiological uas tau pom zoo tias glomerular filtration rate (GFR) thiab RBF tuaj yeem sib txawv ntawm qhov nruab nrab ntawm cov hlab ntsha siab (mABP), tab sis, txawm li cas los xij, qhov cuam tshuam ntawm kev nce mABP ntawm lub raum hemodynamic txawv ntawm tus kheej [ 58] ib. Hauv kev sim 65, ib lub tswv yim ntawm kev tso cai hypotension zoo piv rau kev saib xyuas ib txwm muaj rau cov neeg mob hnub nyoog 65 xyoo lossis tshaj saud thiab tau mus rau ICU rau vasodilatory hypotension tau sim. Tsis muaj qhov sib txawv tau pom zoo nrog rau qhov tshwm sim ntawm RRT, suav nrog cov pab pawg ntawm cov neeg mob uas muaj keeb kwm mob ntshav siab [59]. Txawm li cas los xij, qhov tsis muaj qhov sib txawv no yuav tsum tau txhais nrog ceev faj vim qhov sib txawv me me hauv mABP theem ntawm cov pab pawg (feem ntau mABP ntawm 67 [64-70] mmHg thiab mABP ntawm 73 [69–76] mmHg). Hauv lwm tus neeg hauv ICU, cov xwm txheej tsis zoo rau lub raum tsis tshua pom nyob rau hauv cov neeg mob siab (4 vs. 9 feem pua, p=0.002) hauv RCT suav nrog cov neeg mob tau txais mus rau ICU rau qhov mob hnyav intracerebral hemorrhage [60]. Ua ke, cov kev tshawb pom no tseem tsis tau txhawb nqa kev siv ntau dua ntawm mABP lub hom phiaj hauv cov neeg mob poob siab los tiv thaiv lub raum. Txawm li cas los xij, physiological kev tshawb fawb qhia tau hais tias glomerular pom tus nqi thiab lub raum cov ntshav ntws tuaj yeem sib txawv thoob plaws mABP ntau yam thiab qhov cuam tshuam ntawm kev nce mABP ntawm lub raum hemodynamic sib txawv ntawm tus kheej [58].

Thaum lub sij hawm poob siab, nws tau pom zoo tias qhov txo qis hauv cov ntshav siab qis dua qhov kev txwv ntawm lub raum tus kheej tswj lub peev xwm ua rau yuav luag tawm hauv RBF. Thaum norepinephrine tseem yog thawj-xaiv vasopressor los tswj cov hlab ntsha perfusion, nws cov teebmeem ncaj qha ntawm RBF tseem muaj teeb meem. Ntawm ib sab, norepinephrine tau pom tias yuav txo qis RBF hauv cov neeg ua haujlwm noj qab haus huv thiab nws cov kev cuam tshuam nephrotoxic feem ntau yog siv rau hauv kev tshawb fawb tseem ceeb ntawm cov qauv tsiaj los txhawb AKI [61, 62]. Ntawm qhov tod tes, nyob rau hauv kev faib tawm, kev siv norepinephrine restores RBF [58, 63]. Vasopressin tau pom zoo los txhim kho lub raum cov txiaj ntsig hauv cov ntawv qhia ua ntej. Txawm li cas los xij, vasopressin tseem tsis tau pom zoo dua rau norepinephrine hauv kev tiv thaiv AKI hauv ICU cov neeg mob [64–66].
Txhim kho cov pa oxygen / xav tau kev sib npaug Ntau ntau lwm cov txheej txheem txhawm rau txhim kho intrarenal perfusion lossis oxygenation tau raug soj ntsuam, suav nrog rau lub raum vasodilators, tswj lub raum hypercatabolism, tshuaj tiv thaiv kab mob, thiab tshuaj antioxidants. Ntawm lawv, dopamine yog undoubtedly qhov feem ntau kawm ib tug. Nws cov thawj coj ntawm cov koob tshuaj tsawg (<5 µg/kg/min)="" induces="" special="" dopaminergic="" and="" β-adrenergic="" effects="" and="" therefore="" causes="" renal="" vasodilatation.="" however,="" despite="" intensive="" research="" for="" more="" than="" 30="" years,="" data="" remain="" largely="" inconclusive="" to="" prevent="" the="" occurrence="" of="" aki="" [67].="" other="" vasodilators="" agents,="" like="" fenoldopam,="" b-type="" natriuretic="" peptide,="" and="" levosimendan,="" have="" failed="" to="" show="" any="" renal="" benefit="" [68–71].="" erythropoietin,="" steroids,="" tight="" glucose="" control,="" and="" numerous="" metabolic="" interventions="" have="" also="" been="" used="" to="" prevent="" kidney="" damage="" in="" various="" conditions.="" except="" for="" the="" control="" of="" blood="" glucose="" level="" for="" which="" conflicting="" results="" have="" been="" obtained="" [72,="" 73],="" no="" real="" benefit="" has="" been="" observed="" with="" these="" metabolic="" interventions="" as="" well="">5>
Bundles Tshaj li ib qho kev cuam tshuam, "bundles" tau raug npaj los tiv thaiv AKI [77, 78]. Cov pob khoom yog ib qho me me, ncaj nraim ntawm cov pov thawj-raws li kev coj ua uas tau ua pov thawj los txhim kho cov txiaj ntsig ntawm tus neeg mob thaum ua tau zoo thiab muaj kev ntseeg siab (Daim duab 2). Qhov no zoo li tso cai rau kev paub zoo dua [79] thiab txo qhov kev pheej hmoo ntawm AKI kev nce qib [80]. Kev siv cov pob khoom tau tuaj yeem ua kom pom qhov txo qis ntawm qhov tshwm sim ntawm AKI hauv cov chaw tshwj xeeb xws li nephrotoxic AKI lossis kev phais mob tom qab mob plawv [81, 82]. Txawm hais tias siv cov pob khoom no hauv ICU cov pej xeem lossis hauv sepsis tuaj yeem tiv thaiv AKI tseem tsis paub.
Thaum lub sij hawm AKI: txhim kho kev rov qab los thaum ntxov los ntawm AKI Kev Ua Haujlwm ntawm PGC1 -NAD txoj hauv kev Thaum tsis muaj kev kho mob tshwj xeeb ntawm AKI tseem muaj, ntau qhov kev nkag siab ntawm cov txheej txheem ua rau AKI hauv ischemic lossis septic mob tau ua rau xyoo tas los. Ntawm lawv, PPAR Gamma Coactivator 1 alpha Nicotinamide Adenine Dinucleotide (PGC1 -NAD) txoj kev yog ib lub hom phiaj zoo tshaj plaws rau AKI. Raws li lub raum proximal tubular hlwb yog ib qho ntawm lub zog tshaj plaws lossis ATP-xav cov hlwb hauv lub cev, lawv nyob ntawm kev ua haujlwm mitochondrial. Kev nce hauv kev qhia ntawm PGC1 hauv lub raum epithelial hlwb raug rau ischemic stress tau pom muaj kev tiv thaiv, nrog nce ntawm NAD ntxiv [83, 84]. Tsis tas li ntawd, kev txo qis ntawm PGC1 tau pom ntawm tib neeg lub raum biopsies hauv cov neeg mob AKI [84]. PPAR agonists tau raug npaj los tiv thaiv AKI induced los ntawm cisplatin lossis ischemia-reperfusion [85, 86]. Thawj chav kawm-kuaj yog fibrates, nrog cov txiaj ntsig sib xyaw [85, 86]. Lwm txoj hauv kev yog txhawm rau txhawm rau oxidation ntawm fatty acid (AF) los ntawm kev txhim kho kev thauj mus los ntawm AF hauv mitochondrial matrix siv koom nrog carnitine thiab tus activator ntawm carnitine palmitoyl-transferase 1 kuj hu ua enzyme ntawm carnitine shuttle [87]. Txawm li cas los xij, cov no yog cov ntaub ntawv tseem ceeb preclinical uas tsis muaj kev ntsuam xyuas hauv cov neeg mob. Nicotinamide (Nam), daim ntawv amine ntawm Vitamin B3 (niacin), tau txheeb xyuas tias yog lub peev xwm stimulator ntawm zus tau tej cov NAD ntxiv [88]. Tom qab cog lus tias kev sim ua ntej, kev tswj hwm ntawm Nam tau raug soj ntsuam hauv kev tiv thaiv tom qab kev phais AKI hauv kev phais plawv hauv ib lub chaw sim nrog kev txhawb nqa [89]. Hauv theem 1 pilot txoj kev tshawb no, 37 tus neeg mob tom qab kev phais plawv tau muab tso rau hauv peb pawg: placebo, nicotinamide 1 g ib hnub, thiab 3 g ib hnub. Cov cheeb tsam nyob rau hauv qhov nkhaus ntawm tag nrho cov longitudinal SCr ntsuas tom qab randomization yog siab dua nyob rau hauv cov placebo pawg vs cov neeg mob uas tau txais nicotinamide supplementation. Thaum cov txiaj ntsig no tsim nyog rov ntsuas dua hauv cov qauv loj dua nrog cov txiaj ntsig tsim nyog, cov ntaub ntawv tawm tshiab txuas NAD ntxiv rau qhov sib npaug rau AKI tsis kam qhib tshooj tshiab tshiab hauv AKI tshawb fawb [88, 90].

Kev kho lub raum hloov: lub sijhawm rau tus neeg mob zoo
The modality and the timing of initiation of RRT impact renal outcome. Concerning the modalities, it has been historically suggested that continuous techniques are associated with better hemodynamic stability [91]. Continuous RRT (CRRT) appears to result in fewer hypotension episodes during RRT sessions, allowing better renal perfusion, and, therefore, better recovery of renal function [92], potentially due to lower ultrafiltration rate and lower osmotic shifts compared to IHD [93]. After identifying 6,627 patients treated by RRT in ICU and survivors at day 90, Wald et al. were able to compare 2,004 patients treated with CRRT with 2,004 patients treated with intermittent hemodialysis (IHD) using a propensity score matching. Patients treated with IHD vs. CRRT were at higher risk of ESRD at 90 days (8.2 per 100 patient-years vs. 6.5 per 100 patient-year; HR=0.75 [0.65–0.87]) [94]. However, these results were not confirmed in a subsequent study, which included 638 patients admitted to a single tertiary care academic medical center for 8 years and treated with RRT. After applying a conditional logistic regression model stratified by propensity score for CRRT, there was no significantly higher risk of dialysis dependence at day 90 (OR=1.19 [0.91–1.55] for CRRT, p=0.20) and day 365 (OR=0.93 [0.72–1.20] for CRRT, p=0.55). Even if a difference favoring CRRT at day 90 was observed (186/244 (76.2%) for CRRT patients vs. 66/101 (65.3%) for IHD patients, p=0.05), this association did not remain significant at day 365 [95]. Exploration of the French electronic health record revealed an association between the use of IHD and the risk of developing CKD among ICU patients [96]. The KDIGO guidelines suggest the use of CRRT for patients with unstable hemodynamics but with a moderate level of evidence [7] since available RCTs were not designed to address the impact on renal outcome [97]. While the timing of renal replacement therapy does not affect survival in critically ill patients [98–102], data suggest the potential harm of liberal use of RRT on renal recovery. No difference in renal recovery was observed at day 90 in both the ELAIN study (9/67 (13.4%) for the early group vs. 8/53 (15.1%) for the delayed group, p=0.80) and the IDEALICU trial (2/101 (2%) for the early group vs. 3/110 (3%) for the delayed group, p>{{0}}.90) [99, 102]. Tsis ntev los no, ntau dua RRT kev vam khom ntawm cov neeg muaj txoj sia nyob rau hnub 90 tau pom nyob rau hauv txoj kev tshawb fawb START-AKI (85/814 (10.4 feem pua) rau cov pab pawg nrawm dua vs. 49/815 (6.0 feem pua) rau pawg qauv). Hais txog cov txiaj ntsig mus ntev, kev tshuaj xyuas los ntawm qhov txuas ntxiv 1- xyoo rov qab los ntawm ELAIN txoj kev tshawb fawb pom tias muaj kev pom zoo ntawm kev pib ntxov ntawm RRT txawm hais tias muaj kev tuag (qhov txawv kiag li - 19.6 (− 32; - 7.2) feem pua. ,ua p<0.01) or="" recovery="" of="" renal="" function="" (absolute="" diference="−" 34.8="" (−="" 54.6;="" −="" 15)="" %,="" p="0.001)">0.01)>

Cistanche muaj txiaj ntsig zoo hauv kev kho mob raum
Tom qab AKI: Tiv thaiv qhov tshwm sim mus sij hawm ntev Lub tswv yim kho tsis zoo thiab kev hloov pauv mus rau lub raum fibrosis Tau ntev, qhov xav tias lub raum qhov txhab ntawm AKI yog mob tubular necrosis (ATN), txwv tsis pub piav raws li ntu ntu nrog kev rov zoo tag nrho. Nws yog tam sim no tsim tau zoo tias kev kho tom qab ATN yog qhov kawg ntawm qhov tsis zoo, ua rau lub tswv yim ntawm "maladaptive kho." Qhov no "maladaptive kho" pib fibrogenesis txawm tias thaum morphology thiab lub raum ua haujlwm tau pom meej rov qab mus rau qhov qub. Ib yam li ntawd, cov pov thawj nce ntxiv hauv kev hloov lub raum qhia tau hais tias lub sijhawm ischemic txuas nrog kev hloov pauv fibrosis [104]. Txog tam sim no, plaub txoj hauv kev tseem ceeb tau raug txheeb xyuas kom ua rau mob fibrosis tom qab ib ntus ntawm AKI ncua sijhawm: (a) epigenetic silencing ntawm RASAL1, ib qho proliferation inhibitor, hauv myofibroblasts; (b) lub voj voog ntawm tes raug ntes hauv G2 / M hauv tubular epithelial hlwb (G2 / M theem yog qhov chaw ua haujlwm ntawm cov epithelial ze dua rau ib qho mesenchymal); (c) down-regulation ntawm FA oxidation nyob rau hauv tubular epithelial hlwb [105–107]; thiab ua kom cov renin-angiotensin-aldosterone system (SRAA) [108–110].
Thaiv lub renin-angiotensin system los tiv thaiv fibrogenesis Ua kom SRAA yog ib txoj hauv kev tseem ceeb rau kev txhim kho cov kab mob plawv. Angiotensin II (AngII) tau pom tias ua rau cytokine secretion los ntawm tubular hlwb thiab txhawb cov tsub zuj zuj ntawm inflammatory cells nyob rau hauv ob lub tubular thiab glomerular compartments [108]. Te MD2/TLR4/MyD88 plays lub luag haujlwm tseem ceeb hauv kev kho cov teebmeem ntawm AngII [109]. Kev puas tsuaj ntxiv rau lub raum yuav tshwm sim los ntawm kev ua kom cov coagulation cascade thiab leucocyte adhesion hauv microvessels [111]. Reciprocally, antagonization ntawm AngII confers raum kev tiv thaiv nyob rau hauv ib tug qauv ntawm subtotal nephrectomy nyob rau hauv nas [110]. Tsis xav tsis thoob, AngII tau siv dav los txhim kho qhov pib ntawm lub raum raug mob hauv cov qauv tsiaj. Tsis tas li ntawd, cov ntaub ntawv muaj zog qhia tau hais tias AngII yog qhov tseem ceeb rau kev loj hlob ntawm lub raum fibrosis thiab mob raum kab mob los ntawm cov ntaub so ntswg o thiab matrix protein deposition [109]. Hloov pauv, qee qhov kev sim ua haujlwm tau qhia tias qhov tsis txaus ntawm SRAA kev ua haujlwm, pab txhawb rau vasoplegia thaum muaj kev poob siab [112]. AngII tau raug tshawb xyuas los kho cov ntshav siab hauv cov neeg mob ntawm cov tshuaj vasopressors siab hauv RCT tsis ntev los no [113]. Txawm li cas los xij, qhov kev ntsuas mus sij hawm ntev, tshwj xeeb tshaj yog hais txog qhov tshwm sim ntawm CKD hauv cov neeg muaj sia nyob, tseem tsis tau ua tiav, tshwj xeeb tshaj yog cov neeg mob kho rau lub sijhawm ntev [114].
Ntawm qhov tod tes, ntau qhov kev soj ntsuam cov ntaub ntawv qhia tias muaj txiaj ntsig zoo ntawm kev thaiv SRAA hauv cov neeg mob rov qab los ntawm AKI. Hauv ib pawg ntawm 611 cov neeg mob nrog AKI thaum lub sijhawm ICU nyob thiab tso tawm ciaj sia los ntawm ICU, qhov muaj SRAA inhibitor ntawm ICU tso tawm tau cuam tshuam nrog kev tuag qis dua nrog cov qhab nia sib npaug ntawm qhov phom sij ntawm 0.48 [{{4 }}.27–0.85], ib<0.01) [115].="" similar="" results="" were="" observed="" in="" another="" large="" canadian="" cohort,="" including="" 46,253="" patients="" who="" suffered="" aki="" during="" hospitalization.="" blocking="" sraa="" was="" associated="" with="" better="" outcomes="" at="" 2="" years="" (hr="0.85" [0.81–0.89],="">0.01)><0.01) but="" was="" not="" associated="" with="" esrd="" or="" composite="" outcome="" composed="" by="" esrd="" or="" sustained="" doubling="" of="" serum="" creatinine="" [116].="" these="" results="" were="" not="" observed="" in="" an="" ancillary="" study="" of="" the="" akiki="" trial,="" which="" failed="" to="" evidence="" any="" beneficial="" association="" between="" sraa="" blockers="" and="" 2-years="" outcomes="" in="" kdigo3="" survivors="" [117].="" of="" note,="" this="" study="" was="" likely="" to="" lack="" power.="" no="" increased="" risk="" of="" recurrent="" hospitalized="" aki="" was="" observed="" after="" the="" new="" use="" of="" sraa="" blockers="" suggesting="" that="" starting="" or="" resuming="" these="" medications="" is="" safe="" after="" aki="" [118,="">0.01)>
Ua raws li kev soj ntsuam rov qab rau cov neeg mob 3 lub hlis tom qab AKI tau pom zoo los ntawm KDIGO cov lus qhia [7], ntau qhov kev tshawb fawb tau hais txog qhov tseeb tias tsuas yog ib feem me me ntawm cov neeg mob thaum kawg tau txais txiaj ntsig los ntawm qhov kev ntsuam xyuas no. Cov ntaub ntawv muaj qhia tau hais tias tsawg dua 30 feem pua ntawm cov neeg mob uas raug mob AKI thaum mus pw hauv tsev kho mob raug tshuaj xyuas dua hauv thawj xyoo tom qab tso tawm, suav nrog cov neeg mob CKD lossis cov ntshav qab zib uas twb muaj lawm [120, 121], txawm tias tam sim no pom zoo los ntawm nephrologists [122]. Txawm li cas los xij, qhov kev soj ntsuam zoo li no yuav cuam tshuam qhov tshwm sim los ntawm kev ua kom zoo ntawm kev kho mob, kev kuaj pom, thiab kev tiv thaiv kab mob plawv thiab kev tiv thaiv cov ntu tshiab ntawm AKI. Hauv kev tshawb fawb Ontario pej xeem, 3,877 tus neeg mob uas raug kev txom nyem AKI kho los ntawm kev kho lub raum hloov thiab tawm hauv tsev kho mob tau raug soj ntsuam nyob ntawm qhov ua tiav ntawm kev sib tham tom qab [123]. Kev mus ntsib kws kho mob nephrologist hauv 90 hnub tom qab tso tawm tau cuam tshuam nrog 24 feem pua ntawm cov neeg tuag tom qab 2 xyoos tom qab. Txawm li cas los xij, nrog kev nce hauv tsev kho mob tus nqi nyuaj los ntawm AKI, kev siv dav dav ntawm kev ntsuas rov qab tuaj yeem tshaj qhov muaj peev xwm ntawm cov kev pab cuam nephrology. Muab qhov txiaj ntsig tsis zoo ntawm AKI cov neeg muaj sia nyob, RCT thiab cov kev tshawb fawb soj ntsuam yav tom ntej, raws li kev kawm txuas ntxiv ntawm Fab Kis PREDICT multicenter [124], yuav tsum tau txiav txim siab seb cov neeg mob twg yuav tau txais txiaj ntsig zoo tshaj plaws los ntawm cov kev cuam tshuam no.
Kev pom ntawm AKI kev tshawb fawb: qhov chaw ua si zoo kawg ntawm kev kis mob, kev tshawb fawb yooj yim, thiab kev tshawb fawb txhais lus
Nyob rau hauv xyoo tas los no, vim qhov kev nthuav dav ntawm cov ntaub ntawv loj, cov txuj ci txuj ci dag dag (AI) tau nce qhov tseem ceeb hauv kev saib xyuas tseem ceeb. AKI tsis raug zam los ntawm kev siv cov txuj ci AI, tshwj xeeb, los kwv yees qhov tshwm sim AKI lossis ua rau hnyav dua [125–129]. Cov qauv kev kawm tob tsim los ntawm cov ntaub ntawv kho mob hauv hluav taws xob los ntawm 703,782 cov neeg mob laus tuaj yeem kwv yees li 55.8 feem pua ntawm tag nrho cov ntu ntawm AKI, 90.2 feem pua ntawm tag nrho AKI yuav tsum tau lim ntshav, nrog rau lub sijhawm ua haujlwm ntev txog 48 teev thiab qhov piv ntawm 2 kev ceeb toom tsis tseeb rau txhua qhov tiag. ceeb toom [125]. Txawm li cas los xij, qhov kev txwv loj ntawm cov qauv no yog tias qhov kev kwv yees ntawm AKI tau muab los ntawm kev hloov pauv hauv SCr, uas tseem yog qhov cim tsis zoo rau lub raum ua haujlwm [130].
Txog niaj hnub no, kev tshawb fawb txog kev lom neeg tshiab (plasmatic lossis urinary NGAL, KIM{{{0}}}, Cystatin C, TIMP-2, IGFBP7) lossis cov cim tsis yog lom (intra-renal Doppler flow indices) ntawm lub raum raug mob sawv cev ib feem tseem ceeb ntawm cov ntaub ntawv nrog cov txiaj ntsig tsis sib xws. Tsis yog pab hauv kev kuaj mob ntawm AKI, lawv tuaj yeem muaj txiaj ntsig zoo hauv kev kwv yees cov hom mob hnyav tshaj plaws ntawm AKI [131] lossis kuaj pom kev raug mob raum hauv cov neeg mob tsis tau raws li cov ntsiab lus tam sim no ntawm AKI (xws li hu ua sub-clinical AKI). Yog hais tias ob qho tib si RCTs AKIKI thiab IDEAL-ICU tsis tau ua kom pom kev muaj sia nyob ben eft raws li lub sijhawm pib ntawm RRT rau txhua tus neeg mob nrog theem 3 AKI, qhov kev tuag siab tau pom nyob rau hauv cov neeg mob uas tau txais RRT tom qab ua pov thawj qhov xav tau los txheeb xyuas qhov pheej hmoo AKI [ 98, 99] ib. Nyob rau hauv ib qho kev tshawb fawb txog kev soj ntsuam hauv ntau lub teb chaws, Hoste et al. tau txheeb xyuas thawj zaug ntawm cov zis tshiab biomarker, C-C motif chemokine ligand 14 (CCL14), nrog kev ntxub ntxaug zoo (AUC=0.83 [0.78–0.87]) [132] . Yog tias qhov kev tshawb pom ntawm CCL14 raws li kev kwv yees tsis tu ncua AKI tsis yog thawj tus qhia lub luag haujlwm ntawm monocytes / macrophages hauv pathophysiology ntawm AKI, tshwj xeeb tshaj yog nyob rau hauv sepsis [133], nws muaj lub sijhawm los txheeb xyuas txoj hauv kev tshiab ntawm AKI kho. Ntxiv mus, cov lus cog tseg ntawm kev cuam tshuam thaum ntxov tuaj yeem txhim kho lub raum cov txiaj ntsig hauv infraclinic AKI yuav tsum tau txhawb nqa los ntawm kev txhim kho biomarkers kev tshawb fawb.
Qhov cuam tshuam ntawm cov tswv yim ntawm RRT ntawm lub raum rov qab tseem tsis to taub thiab yuav tsum tau tshawb nrhiav. Thaum kawg, cov tswv yim los tiv thaiv kev txhim kho mus sij hawm ntev ntawm ob qho tib si mob thiab cov kab mob plawv yuav tsum tau ua tib zoo saib xyuas kom txo qis AKI "scar".
Thaum kawg, tom qab kho kho tshiab, xyoo tom ntej yuav nthuav tawm cov ntsiab lus kawg tshiab uas yuav tso cai rau peb los txhais cov ntsiab lus ntawm kev txaus siab hauv qhov chaw ntawm AKI (Table 1), zoo dua qhia txog qhov muaj feem ntau ntawm AKI / CKD / ESRD thiab tag nrho cov ciaj sia taus, thiab txhim kho peb. cov cuab yeej los ntsuas GFR lub sijhawm tiag tiag, lub raum ua haujlwm, thiab lub raum puas.

Cistanche muaj txiaj ntsig zoo hauv kev kho mob raum & tiv thaiv qog noj ntshav
Xaus
AKI muaj ntau heev ntawm cov neeg mob ICU thiab tau cuam tshuam nrog cov txiaj ntsig luv luv thiab ntev. Ntau lub tswv yim kho mob tuaj yeem tiv thaiv lossis txo qhov tshwm sim ntawm AKI. Cov kev tshawb fawb yav tom ntej yuav tsum tam sim no txheeb xyuas cov sub-phenotypes ntawm AKI nrog cov lus teb sib txawv rau cov kev kho mob, cov cuab yeej rau kev paub ua ntej thiab zoo dua ntawm lub raum kev puas tsuaj thiab lub raum ua haujlwm, thiab cov tswv yim kho tshiab nrog lub hom phiaj kawg ntawm kev txhim kho cov txiaj ntsig ntawm tus neeg mob.
Xa musnces
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8. Hoste EAJ, Bagshaw SM, Bellomo R, Cely CM, Colman R, Cruz DN, et al. Kev kis kab mob ntawm lub raum mob hnyav hauv cov neeg mob hnyav: kev tshawb fawb ntau lub teb chaws AKI-EPI. Intensive Care Med. 2015; 41(8):1411–23.
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11. Honore PM, Jacobs R, Joannes-Boyau O, De Regt J, Boer W, De Waele E, et al. Septic AKI hauv ICU cov neeg mob. Kev kuaj mob, pathophysiology, thiab hom kev kho mob, koob tshuaj, thiab sijhawm: kev tshuaj xyuas dav dav ntawm kev txhim kho tsis ntev los no thiab yav tom ntej. Ann Intensive Care. 2011; 1(1):32.
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13. Drolz A, Horvatits T, Roedl K, Rutter K, Staufer K, Haider DG, et al. Cov txiaj ntsig thiab cov yam ntxwv ntawm mob raum raug mob ua rau muaj teeb meem hypoxic hepatitis ntawm chav kho mob hnyav. Ann Intensive Care. 2016; 6(1):61.
14. Panitchote A, Mehkri O, Hastings A, Hanane T, Demirjian S, Torbic H, et al. Cov xwm txheej cuam tshuam nrog mob raum raug mob hauv cov mob ua pa nyuaj. Ann Intensive Care. Xyoo 2019; 9(1): 74.
15. Darmon M, Vincent F, Canet E, Mokart D, Pène F, Kouachet A, et al. Mob raum raug mob hauv cov neeg mob hnyav nrog cov kab mob haematological malignancies: cov txiaj ntsig ntawm kev tshawb fawb multicentre cohort los ntawm Pawg de Recherche en Réanimation Respiratoire en Onco-Hématologie. Nephrol Dial Hloov Ntawm Publ Eur Dial Transpl Assoc Eur Ren Assoc. 2015; 30(12): 2006–13.
